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Article: Application of immuno- and affinity labeling with fluorescent dyes to in-resin CLEM of Epon-embedded cells.

Tanida, Isei / Yamaguchi, Junji / Suzuki, Chigure / Kakuta, Soichiro / Uchiyama, Yasuo

2023 Volume 9, Issue 6, Page(s) e17394

Abstract: In-resin CLEM (Correlative Light and Electron Microscopy) of Epon-embedded cells involves correlating fluorescence microscopy with electron microscopy in the same Epon-embedded ultrathin section. This method offers the advantage of high positional ... ...

Abstract	In-resin CLEM (Correlative Light and Electron Microscopy) of Epon-embedded cells involves correlating fluorescence microscopy with electron microscopy in the same Epon-embedded ultrathin section. This method offers the advantage of high positional accuracy compared to standard CLEM. However, it requires the expression of recombinant proteins. In order to detect the localization of endogenous target(s) and their localized ultrastructures of Epon-embedded samples using in-resin CLEM, we investigated whether immunological and affinity-labeling using fluorescent dyes applied to in-resin CLEM of Epon-embedded cells. The orange fluorescent (λ
Language	English
Publishing date	2023-06-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e17394
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Article ; Online: Recent advances in in-resin correlative light and electron microscopy of Epon-embedded cells.

Tanida, Isei / Yamaguchi, Junji / Suzuki, Chigure / Kakuta, Soichiro / Uchiyama, Yasuo

Microscopy (Oxford, England)

2023 Volume 72, Issue 5, Page(s) 383–387

Abstract: Correlative fluorescent and electron microscopic images of the same section of epoxy (or other polymer)-embedded samples, hereafter referred to as 'in-resin CLEM', have been developed to improve the positional accuracy and Z-axis resolution limitations ... ...

Abstract	Correlative fluorescent and electron microscopic images of the same section of epoxy (or other polymer)-embedded samples, hereafter referred to as 'in-resin CLEM', have been developed to improve the positional accuracy and Z-axis resolution limitations of conventional correlative light and electron microscopy (CLEM). High-pressure freezing and quick-freezing substitution result in in-resin CLEM of acrylic-based resin-embedded cells expressing green fluorescent protein, yellow fluorescent protein, mVenus and mCherry, which are sensitive to osmium tetroxide. The identification of osmium-resistant fluorescent proteins leads to the development of in-resin CLEM of Epon-embedded cells. Using subtraction-based fluorescence microscopy with a photoconvertible fluorescent protein, mEosEM-E, its green fluorescence can be observed in thin sections of Epon-embedded cells, and two-color in-resin CLEM using mEosEM-E and mScarlet-H can be performed. Green fluorescent proteins, CoGFP variant 0 and mWasabi, and far-red fluorescent proteins, mCherry2 and mKate2, are available for in-resin CLEM of Epon-embedded cells using the standard procedure for Epon-embedding with additional incubation. Proximity labeling is applied to in-resin CLEM to overcome the limitations of fluorescent proteins in epoxy resin. These approaches will contribute significantly to the future of CLEM analysis.
MeSH term(s)	Humans ; Epoxy Resins ; Microscopy, Electron ; Microscopy, Fluorescence/methods ; Green Fluorescent Proteins ; HeLa Cells
Chemical Substances	Epoxy Resins ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2023-10-03
Publishing country	England
Document type	Journal Article
ZDB-ID	2707496-1
ISSN	2050-5701 ; 2050-5698
ISSN (online)	2050-5701
ISSN	2050-5698
DOI	10.1093/jmicro/dfad028
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Article ; Online: TUNEL-positive structures in activated microglia and SQSTM1/p62-positive structures in activated astrocytes in the neurodegenerative brain of a CLN10 mouse model.

Mitsui, Shun / Yamaguchi, Junji / Suzuki, Chigure / Uchiyama, Yasuo / Tanida, Isei

Glia

2023 Volume 71, Issue 12, Page(s) 2753–2769

Abstract: Neuronal ceroid lipofuscinosis is a group of pediatric neurodegenerative diseases. One of their causative genes, CLN10/CtsD, encodes cathepsin D, a major lysosomal protease. Central nervous system (CNS)-specific CtsD-deficient mice exhibit a ... ...

Abstract	Neuronal ceroid lipofuscinosis is a group of pediatric neurodegenerative diseases. One of their causative genes, CLN10/CtsD, encodes cathepsin D, a major lysosomal protease. Central nervous system (CNS)-specific CtsD-deficient mice exhibit a neurodegenerative disease phenotype with accumulation of ceroid lipofuscins, granular osmiophilic deposits, and SQSTM1/p62. We focused on activated astrocytes and microglia in this neurodegenerative mouse brain, since there are few studies on the relationship between these accumulators and lysosomes in these glial cells. Activated microglia and astrocytes in this mouse thalamus at p24 were increased by approximately 2.5- and 4.6-fold compared with the control, while neurons were decreased by approximately half. Granular osmiophilic deposits were detected in microglial cell bodies and extended their processes in the thalamus. LAMP1-positive lysosomes, but not SQSTM1/p62 aggregates, accumulated in microglia of this mouse thalamus, whereas both lysosomes and SQSTM1/p62 aggregates accumulated in its astrocytes. TUNEL-positive signals were observed mainly in microglia, but few were observed in neurons and astrocytes. These signals were fragmented DNA from degenerated neurons engulfed by microglia or in the lysosomes of microglia. Abnormal autophagic vacuoles also accumulated in the lysosomes of microglia. Granular osmiophilic deposit-like structures localized to LAMP1-positive lysosomes in CtsD-deficient astrocytes. SQSTM1/p62-positive but LAMP1-negative membranous structures also accumulated in the astrocytes and were less condensed than typical granular osmiophilic deposits. These results suggest that CtsD deficiency leads to intracellular abnormalities in activated microglia and astrocytes in addition to neuronal degeneration.
Language	English
Publishing date	2023-08-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24449
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Zs.A 2345: Show issues

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Article ; Online: Inefficient development of syncytiotrophoblasts in the

Ochiai, Yuki / Suzuki, Chigure / Segawa, Katsumori / Uchiyama, Yasuo / Nagata, Shigekazu

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 18, Page(s) e2200582119

Abstract: The P4-ATPases ATP11A and ATP11C function as flippases at the plasma membrane to translocate phosphatidylserine from the outer to the inner leaflet. We herein demonstrated that Atp11a-deficient mouse embryos died at approximately E14.5 with thin-walled ... ...

Abstract	The P4-ATPases ATP11A and ATP11C function as flippases at the plasma membrane to translocate phosphatidylserine from the outer to the inner leaflet. We herein demonstrated that Atp11a-deficient mouse embryos died at approximately E14.5 with thin-walled heart ventricles. However, the cardiomyocyte- or epiblast-specific Atp11a deletion did not affect mouse development or mortality. ATP11C may have compensated for the function of ATP11A in most of the cell types in the embryo. On the other hand, Atp11a, but not Atp11c, was expressed in the mouse placenta, and the Atp11a-null mutation caused poor development of the labyrinthine layer with an increased number of TUNEL-positive foci. Immunohistochemistry and electron microscopy revealed a disorganized labyrinthine layer with unfused trophoblasts in the Atp11a-null placenta. Human placenta-derived choriocarcinoma BeWo cells expressed the ATP11A and ATP11C genes. A lack of ATP11A and ATP11C eliminated the ability of BeWo cells to flip phosphatidylserine and fuse when treated with forskolin. These results indicate that flippases at the plasma membrane play an important role in the formation of syncytiotrophoblasts in placental development.
MeSH term(s)	ATP Binding Cassette Transporter 1 ; Adenosine Triphosphatases/metabolism ; Animals ; Cell Membrane/metabolism ; Female ; Mice ; Phosphatidylserines/metabolism ; Placenta/metabolism ; Pregnancy ; Trophoblasts/metabolism
Chemical Substances	ABCA1 protein, mouse ; ATP Binding Cassette Transporter 1 ; Phosphatidylserines ; Adenosine Triphosphatases (EC 3.6.1.-)
Language	English
Publishing date	2022-04-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2200582119
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Zs.A 1148: Show issues

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Article ; Online: Infertility Caused by Inefficient Apoptotic Germ Cell Clearance in

Yamashita, Yahiro / Suzuki, Chigure / Uchiyama, Yasuo / Nagata, Shigekazu

Molecular and cellular biology

2020 Volume 40, Issue 3

Abstract: During spermatogenesis, up to 75% of germ cells in the testes undergo apoptosis and are cleared by Sertoli cells. X-linked XK blood group-related 8 (Xkr8) is a plasma membrane protein that scrambles phospholipids in response to apoptotic signals, ... ...

Abstract	During spermatogenesis, up to 75% of germ cells in the testes undergo apoptosis and are cleared by Sertoli cells. X-linked XK blood group-related 8 (Xkr8) is a plasma membrane protein that scrambles phospholipids in response to apoptotic signals, exposing phosphatidylserine (PtdSer). Here, we found that
MeSH term(s)	Animals ; Apoptosis ; Apoptosis Regulatory Proteins/genetics ; Gene Deletion ; Germ Cells/cytology ; Germ Cells/metabolism ; Germ Cells/pathology ; Infertility, Male/genetics ; Infertility, Male/pathology ; Infertility, Male/physiopathology ; Male ; Membrane Proteins/genetics ; Mice ; Mice, Inbred C57BL ; Spermatogenesis ; Testis/cytology ; Testis/metabolism ; Testis/pathology
Chemical Substances	Apoptosis Regulatory Proteins ; Membrane Proteins ; Xkr8 protein, mouse
Language	English
Publishing date	2020-01-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.00402-19
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Zs.A 1666: Show issues

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Article ; Online: Infertility Caused by Inefficient Apoptotic Germ Cell Clearance in Xkr8-Deficient Male Mice

Yamashita, Yahiro / Suzuki, Chigure / Uchiyama, Yasuo / Nagata, Shigekazu

Molecular and Cellular Biology. 2020 Jan. 16, v. 40, no. 3 p.e00402-19-

2020

Abstract	During spermatogenesis, up to 75% of germ cells in the testes undergo apoptosis and are cleared by Sertoli cells. X-linked XK blood group-related 8 (Xkr8) is a plasma membrane protein that scrambles phospholipids in response to apoptotic signals, exposing phosphatidylserine (PtdSer). Here, we found that Xkr8 ⁻/⁻ male mice were infertile due to reduced sperm counts in their epididymides. Apoptotic stimuli could not induce PtdSer exposure in Xkr8 ⁻/⁻ germ cells. Consistent with the hypothesis that PtdSer functions as an “eat-me” signal to phagocytes, cells expressing phosphatidylserine receptor TIM4 and MER tyrosine kinase receptor efficiently engulfed apoptotic wild-type male germ cells but not Xkr8 ⁻/⁻ germ cells. Fluorescence and electron microscopy revealed Sertoli cells carrying engulfed and degenerated dead cells. However, many unengulfed apoptotic cells and residual bodies and much cell debris were present in Xkr8 ⁻/⁻ testes and epididymides. These results indicate that Xkr8-mediated PtdSer exposure is essential for the clearance of apoptotic germ cells by Sertoli cells. There was no apparent inflammation in Xkr8 ⁻/⁻ testes, suggesting that the unengulfed apoptotic cells may have undergone secondary necrosis, releasing noxious materials that affected the germ cells. Alternatively, failure to engulf the apoptotic germ cells may have caused the Sertoli cells to starve and lose their ability to support spermatogenesis.
Keywords	apoptosis ; blood ; electron microscopy ; fluorescence ; inflammation ; males ; membrane proteins ; necrosis ; phosphatidylserines ; plasma membrane ; spermatogenesis ; spermatozoa ; tyrosine ; phospholipid scramblase ; Sertoli cells ; male infertility ; Xkr8
Language	English
Dates of publication	2020-0116
Publishing place	Taylor & Francis
Document type	Article ; Online
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.00402-19
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Article ; Online: Lack of Cathepsin D in the central nervous system results in microglia and astrocyte activation and the accumulation of proteinopathy-related proteins.

Suzuki, Chigure / Yamaguchi, Junji / Sanada, Takahito / Oliva Trejo, Juan Alejandro / Kakuta, Souichirou / Shibata, Masahiro / Tanida, Isei / Uchiyama, Yasuo

Scientific reports

2022 Volume 12, Issue 1, Page(s) 11662

Abstract: Neuronal ceroid lipofuscinosis is one of many neurodegenerative storage diseases characterized by excessive accumulation of lipofuscins. CLN10 disease, an early infantile neuronal ceroid lipofuscinosis, is associated with a gene that encodes cathepsin D ( ...

Abstract	Neuronal ceroid lipofuscinosis is one of many neurodegenerative storage diseases characterized by excessive accumulation of lipofuscins. CLN10 disease, an early infantile neuronal ceroid lipofuscinosis, is associated with a gene that encodes cathepsin D (CtsD), one of the major lysosomal proteases. Whole body CtsD-knockout mice show neurodegenerative phenotypes with the accumulation of lipofuscins in the brain and also show defects in other tissues including intestinal necrosis. To clarify the precise role of CtsD in the central nervous system (CNS), we generated a CNS-specific CtsD-knockout mouse (CtsD-CKO). CtsD-CKO mice were born normally but developed seizures and their growth stunted at around postnatal day 23 ± 1. CtsD-CKO did not exhibit apparent intestinal symptoms as those observed in whole body knockout. Histologically, autofluorescent materials were detected in several areas of the CtsD-CKO mouse's brain, including: thalamus, cerebral cortex, hippocampus, and cerebellum. Expression of ubiquitin and autophagy-associated proteins was also increased, suggesting that the autophagy-lysosome system was impaired. Microglia and astrocytes were activated in the CtsD-CKO thalamus, and inducible nitric oxide synthase (iNOS), an inflammation marker, was increased in the microglia. Interestingly, deposits of proteinopathy-related proteins, phosphorylated α-synuclein, and Tau protein were also increased in the thalamus of CtsD-CKO infant mice. Considering these results, we propose thatt the CtsD-CKO mouse is a useful mouse model to investigate the contribution of cathepsin D to the early phases of neurodegenerative diseases in relation to lipofuscins, proteinopathy-related proteins and activation of microglia and astrocytes.
MeSH term(s)	Animals ; Astrocytes/metabolism ; Cathepsin D/genetics ; Cathepsin D/metabolism ; Central Nervous System/metabolism ; Disease Models, Animal ; Humans ; Mice ; Mice, Knockout ; Microglia/metabolism ; Neuronal Ceroid-Lipofuscinoses/pathology
Chemical Substances	Cathepsin D (EC 3.4.23.5) ; Ctsd protein, mouse (EC 3.4.23.5)
Language	English
Publishing date	2022-07-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-15805-3
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Article ; Online: Characterization of starvation-induced autophagy in cerebellar Purkinje cells of pHluorin-mKate2-human LC3B transgenic mice.

Oliva Trejo, Juan Alejandro / Tanida, Isei / Suzuki, Chigure / Kakuta, Soichiro / Tada, Norihiro / Uchiyama, Yasuo

Scientific reports

2020 Volume 10, Issue 1, Page(s) 9643

Abstract: We generated a new transgenic mouse model that expresses a pHluorin-mKate2 fluorescent protein fused with human LC3B (PK-LC3 mice) for monitoring autophagy activity in neurons of the central nervous system. Histological analysis revealed fluorescent ... ...

Abstract	We generated a new transgenic mouse model that expresses a pHluorin-mKate2 fluorescent protein fused with human LC3B (PK-LC3 mice) for monitoring autophagy activity in neurons of the central nervous system. Histological analysis revealed fluorescent puncta in neurons of the cerebral cortex, hippocampus, cerebellar Purkinje cells, and anterior spinal regions. Using CLEM analysis, we confirmed that PK-LC3-positive puncta in the perikarya of Purkinje cells correspond to autophagic structures. To validate the usability of PK-LC3 mice, we quantified PK-LC3 puncta in Purkinje cells of mice kept in normal feeding conditions and of mice starved for 24 hours. Our results showed a significant increase in autophagosome number and in individual puncta areal size following starvation. To confirm these results, we used morphometry at the electron microscopic level to analyze the volume densities of autophagosomes and lysosomes/autolysosomes in Purkinje cells of PK-LC3 mice. The results revealed that the volume densities of autophagic structures increase significantly after starvation. Together, our data show that PK-LC3 mice are suitable for monitoring autophagy flux in Purkinje cells of the cerebellum, and potentially other areas in the central nervous system.
MeSH term(s)	Animals ; Autophagosomes/metabolism ; Autophagy/physiology ; Female ; Green Fluorescent Proteins/metabolism ; Humans ; Luminescent Proteins/metabolism ; Mice, Inbred ICR ; Mice, Transgenic ; Microtubule-Associated Proteins/metabolism ; Purkinje Cells/metabolism ; Purkinje Cells/physiology ; Starvation/metabolism ; Red Fluorescent Protein
Chemical Substances	Luminescent Proteins ; MAP1LC3B protein, human ; Microtubule-Associated Proteins ; PHluorin ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2020-06-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-66370-6
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Article: The sodium–glucose cotransporter 2 inhibitor tofogliflozin prevents diabetic kidney disease progression in type 2 diabetic mice

Li, Zi / Murakoshi, Maki / Ichikawa, Saki / Koshida, Takeo / Adachi, Eri / Suzuki, Chigure / Ueda, Seiji / Gohda, Tomohito / Suzuki, Yusuke

FEBS Open Bio. 2020 Dec., v. 10, no. 12

2020

Abstract: Trials on cardiovascular and renal outcomes in patients with type 2 diabetes have consistently demonstrated that sodium–glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of diabetic kidney disease (DKD) progression. However, their renal ... ...

Abstract	Trials on cardiovascular and renal outcomes in patients with type 2 diabetes have consistently demonstrated that sodium–glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of diabetic kidney disease (DKD) progression. However, their renal protective mechanisms have yet to be completely understood and the effect on albuminuria reduction in animal models is controversial. We investigated these issues using KK and KK‐Aʸ mice as a control (CTRL) and as a model for type 2 diabetes (DKD), respectively. KK‐Aʸ mice were treated with 0.015% tofogliflozin, which is an SGLT2 inhibitor, starting at seven weeks of age for eight weeks. Compared with the CTRL mice, the DKD mice had higher HbA1c levels and albuminuria. Although tofogliflozin treatment significantly lowered HbA1c levels, it did not reverse albuminuria. Tofogliflozin treatment enhanced damage in both the glomerular (i.e., enlarged mesangial area, increased foot process effacement rate, and decreased number of WT‐1‐positive cells) and tubulointerstitial (increased protein levels of KIM‐1 and MCP‐1, increased number of macrophages, and abnormal mitochondrial morphology) areas. Our results suggest that tofogliflozin may prevent glomerular and tubulointerstitial damage, partly by ameliorating hyperglycemia, renal inflammation, and abnormal mitochondrial morphology.
Keywords	albuminuria ; animals ; disease progression ; hyperglycemia ; inflammation ; kidney diseases ; macrophages ; mitochondria ; models ; noninsulin-dependent diabetes mellitus ; risk reduction ; sodium glucose cotransporter-2 inhibitors ; symporters
Language	English
Dates of publication	2020-12
Size	p. 2761-2770.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	JOURNAL ARTICLE
ZDB-ID	2651702-4
ISSN	2211-5463
ISSN	2211-5463
DOI	10.1002/2211-5463.13014
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Article ; Online: Autophagy Deficiency in Renal Proximal Tubular Cells Leads to an Increase in Cellular Injury and Apoptosis under Normal Fed Conditions.

Suzuki, Chigure / Tanida, Isei / Oliva Trejo, Juan Alejandro / Kakuta, Soichiro / Uchiyama, Yasuo

International journal of molecular sciences

2019 Volume 21, Issue 1

Abstract: Renal proximal tubular epithelial cells are significantly damaged during acute kidney injury. Renal proximal tubular cell-specific autophagy-deficient mice show increased sensitivity against renal injury, while showing few pathological defects under ... ...

Abstract	Renal proximal tubular epithelial cells are significantly damaged during acute kidney injury. Renal proximal tubular cell-specific autophagy-deficient mice show increased sensitivity against renal injury, while showing few pathological defects under normal fed conditions. Considering that autophagy protects the proximal tubular cells from acute renal injury, it is reasonable to assume that autophagy contributes to the maintenance of renal tubular cells under normal fed conditions. To clarify this possibility, we generated a knock out mouse model which lacks Atg7, a key autophagosome forming enzyme, in renal proximal tubular cells (
MeSH term(s)	Aging ; Animals ; Apoptosis ; Autophagy ; Autophagy-Related Protein 7/deficiency ; Autophagy-Related Protein 7/genetics ; Hepatitis A Virus Cellular Receptor 1/metabolism ; Kidney/metabolism ; Kidney/pathology ; Kidney Tubules, Proximal/cytology ; Kidney Tubules, Proximal/metabolism ; Kidney Tubules, Proximal/ultrastructure ; Mice ; Mice, Knockout ; Microtubule-Associated Proteins/metabolism ; Sequestosome-1 Protein/metabolism
Chemical Substances	Atg7 protein, mouse ; Havcr1 protein, mouse ; Hepatitis A Virus Cellular Receptor 1 ; Map1lc3b protein, mouse ; Microtubule-Associated Proteins ; Sequestosome-1 Protein ; Sqstm1 protein, mouse ; Autophagy-Related Protein 7 (EC 6.2.1.45)
Language	English
Publishing date	2019-12-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21010155
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